title: Evaluation of the host response in various models of induced periodontal disease in mice.
abstract: BACKGROUND
  The aim of this study is to characterize and evaluate the host response caused by three different models of experimental periodontitis in mice.
  
  
  METHODS
  C57BL/6 wild-type female mice were distributed into six experimental groups and sacrificed at 7, 15, and 30 days after the induction of periodontal disease: 1) group C: no treatment control group; 2) group L: periodontal disease induced by ligature; 3) group G-Pg: oral gavage with Porphyromonas gingivalis (Pg); 4) group G-PgFn: oral gavage with Fusobacterium nucleatum + Pg; 5) group I-Pg: heat-killed Pg injected into the palatal mucosa between the molars; and 6) group I-V: phosphate-buffered saline injected into the palatal mucosa. The samples were used to analyze the immune-inflammatory process in the gingival tissue via descriptive histologic and real-time polymerase chain reaction analyses. The alveolar bone loss was evaluated using microcomputed tomography. The data were analyzed using the Kruskal-Wallis test, followed by a post hoc Dunn test and analysis of variance, followed by a Tukey test using a 5% significance level.
  
  
  RESULTS
  Only the ligature model displayed significant alveolar bone loss in the initial period (7 days), which was maintained with time. The group injected with heat-killed Pg displayed significant alveolar bone loss starting from day 15, which continued to progress with time (P <0.05). A significant increase (P <0.05) in the gene expression of proinflammatory cytokines (interleukin-6 and -1β) and proteins involved in osteoclastogenesis (receptor activator of nuclear factor-κB ligand and osteoprotegerin) was observed in the ligature group on day 7.
  
  
  CONCLUSIONS
  The ligature and injection of heat-killed Pg models were the most representative of periodontal disease in humans, whereas the oral gavage models were not effective at inducing the disease under the experimental conditions.
authors.affiliation: Department of Diagnosis and Surgery, School of Dentistry at Araraquara, Univ Estadual Paulista-UNESP, Araraquara, São Paulo, Brazil.
authors.forename: Rafael Scaf
authors.initials: RS
authors.lastname: de Molon
authors.forename: Erica Dorigatti
authors.initials: ED
authors.lastname: de Avila
authors.forename: Andressa Vilas
authors.initials: AV
authors.lastname: Boas Nogueira
authors.forename: Joao Antonio
authors.initials: JA
authors.lastname: Chaves de Souza
authors.forename: Mario Julio
authors.initials: MJ
authors.lastname: Avila-Campos
authors.forename: Cleverton Roberto
authors.initials: CR
authors.lastname: de Andrade
authors.forename: Joni Augusto
authors.initials: JA
authors.lastname: Cirelli
mesh_terms: D000284:Administration, Oral; D016301:Alveolar Bone Loss / Q000276:immunology / Q000382:microbiology; D000818:Animals; D060085:Coinfection / Q000276:immunology; D018450:Disease Progression; D005260:Female; D016967:Fusobacterium nucleatum / Q000502:physiology; D054884:Host-Pathogen Interactions; D018836:Inflammation Mediators / Q000276:immunology; D007267:Injections; D053583:Interleukin-1beta / Q000032:analysis; D015850:Interleukin-6 / Q000032:analysis; D007962:Leukocytes / Q000276:immunology; D008264:Macrophages / Q000276:immunology; D051379:Mice; D008810:Mice, Inbred C57BL; D009061:Mouth Mucosa / Q000382:microbiology; D010010:Osteoclasts / Q000276:immunology; D053244:Osteoprotegerin / Q000032:analysis; D017622:Periodontal Attachment Loss / Q000276:immunology / Q000382:microbiology; D010518:Periodontitis / Q000276:immunology* / Q000382:microbiology; D016966:Porphyromonas gingivalis / Q000502:physiology; D053245:RANK Ligand / Q000032:analysis; D011897:Random Allocation; D013997:Time Factors; D055114:X-Ray Microtomography / Q000379:methods
chemical_list: D018836:Inflammation Mediators; D053583:Interleukin-1beta; D015850:Interleukin-6; D053244:Osteoprotegerin; D053245:RANK Ligand; C506031:Tnfrsf11b protein, mouse; C505689:Tnfsf11 protein, mouse